ReviewCurrent psychiatry reports2007
Genetics of bipolar disorder.
Review in Current psychiatry reports, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 25 citations in OpenAlex.
- Cognitive manic symptoms in bipolar disorder associated with polymorphisms in the DAOA and COMT genes.PloS one · 2013Article
- Linkage disequilibrium mapping of the chromosome 6q21-22.31 bipolar I disorder susceptibility locus.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2010Article
- The genetics of bipolar disorder.Neuroscience · 2009Review
- Effect of the G72 (DAOA) putative risk haplotype on cognitive functions in healthy subjects.BMC psychiatry · 2009Article
- Alternatively Spliced Genes as Biomarkers for Schizophrenia, Bipolar Disorder and Psychosis: A Blood-Based Spliceome-Profiling Exploratory Study.Current pharmacogenomics and personalized medicine · 2009Article
- Copy variations in schizophrenia and bipolar disorder.Cytogenetic and genome research · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Family and twin studies have consistently documented that bipolar disorder (BPD) is familial and heritable, but efforts to identify specific susceptibility genes have been complicated by the disorder's genetic and phenotypic complexity. Genetic linkage studies have implicated numerous chromosomal regions, but findings have been inconsistent. As with other complex disorders, it has become clear that linkage analysis lacks the power and precision to identify susceptibility loci for BPD. Candidate gene association studies have implicated several specific genes, but these studies have been limited by our incomplete understanding of the disorder's biology, and there have been few robustly replicated results. Within the past 2 years, a major advance in the genetics of complex disease has become feasible in the form of genome-wide association studies. Such studies, which require large sample sizes, have already proven successful in identifying susceptibility variants for a range of common medical disorders. Genome-wide association studies have begun to appear for BPD, and more are in progress. By providing an unbiased approach, this technology may reveal novel biological mechanisms underlying BPD.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.